The limitations in the healing response of the anterior cruciate ligament are well organized. Various reasons have been proposed for the failure of healing of this ligament, particllarly mechanical factors, and nutritional factors resulting from a limited blood supply. It has been proposed that additional harmful effects to repair result from the post-injury synovial fluid which contains numerous proteolytic enzymesarmful to immature proliferaing cells and their matrix. In summary, it is believed that the failure of repair is the result of a multifactorial hostile environment. However, intrinsic repair of flexor tendon in the flexor tendon sheath has been demonstrated in this laboratory when intermittent passive motion is imposed. This environment is seemingly as "hostile" as in the case of the ACL. The blood supply and nutrition are outwardly as limited. Why is intrinsic healing so effective in the case of tendon, but so limited in the case of the ACL? These investigators propose a study to evaluate the early ACL healing response and to compare it to the process of flexor tendon healing. A series of descriptive studies are proposed to clarify differences between the ACL and other ligaments of the knee joint, as well as with flexor tendon with respect to routes of nutririon, repair mechanisms and the influence of activity on repair rate and quality. Subsequent studies will evaluate the routes of nutrition of tissues used in ACL reconstruction, the potential for augmentation of that nutrition by the anterior synovial fat pad, the collagen turnover rate of ligament autograft replacements and the changes in their strength characteristics with time. Nutritional studies will employ labelled collagen precursors (L-5-3H proline) administered by routes chosen to elucidate the questions of nutritional mechanisms. Turnover studies will employ chronic collagen prelabelling. Evaluation of repair mechnanisms will employ a variety of morphological, biomechanical and biochemical techniques.